Quisqualate receptor-mediated depression of calcium currents in hippocampal neurons

Robin A.J. Lester; Craig E. Jahr

doi:10.1016/0896-6273(90)90200-Y

Quisqualate receptor-mediated depression of calcium currents in hippocampal neurons

Robin A.J. Lester
, Craig E. Jahr

Vollum Institute

Research output: Contribution to journal › Article › peer-review

159 Scopus citations

Abstract

The modulation of Ca²⁺ currents by the excitatory neurotransmitter glutamate and its analogs was investigated in hippocampal neurons in culture. In the presence of glutamate receptor-gated ion channel antagonists, all of the analogs tested caused either a small reversible depression or had no effect on the Ca²⁺ current. However, in neurons dialyzed with GTPyS, quisqualate and glutamate but not NMDA, kainate, AMPA, or l-APB caused marked and irreversible depressions of the Ca²⁺ current. This inhibition was only observed if Ca²⁺ was present in either the internal or external medium. Intracellular H-7, staurosporine, IP₃, cAMP, cGMP, or calmodulin inhibitors failed to prevent the quisqualate-induced Ca²⁺ current inhibition. These observations are consistent with an interaction between a G protein-coupled glutamate receptor and Ca²⁺ channels.

Original language	English (US)
Pages (from-to)	741-749
Number of pages	9
Journal	Neuron
Volume	4
Issue number	5
DOIs	https://doi.org/10.1016/0896-6273(90)90200-Y
State	Published - May 1990

Funding

We thank Mr. Jeff Volk for the preparation and maintenance of the neurons and Drs. J. T. Williams and C. L. Westbrook for careful reading and criticism of the manuscript. In separate experiments performed by Dr. M. J. Christie IP, induced an oscillatory Cl-conductance in Xenopus oocytes, confirming the activity of the compound. This work was supported by National Institutes of Health grant NS21419 and the McKnight Endowment Fund for Neuroscience.

Funders	Funder number
Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health
National Institute of Neurological Disorders and Stroke	R01NS021419

ASJC Scopus subject areas

General Neuroscience

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10.1016/0896-6273(90)90200-Y

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title = "Quisqualate receptor-mediated depression of calcium currents in hippocampal neurons",

abstract = "The modulation of Ca2+ currents by the excitatory neurotransmitter glutamate and its analogs was investigated in hippocampal neurons in culture. In the presence of glutamate receptor-gated ion channel antagonists, all of the analogs tested caused either a small reversible depression or had no effect on the Ca2+ current. However, in neurons dialyzed with GTPyS, quisqualate and glutamate but not NMDA, kainate, AMPA, or l-APB caused marked and irreversible depressions of the Ca2+ current. This inhibition was only observed if Ca2+ was present in either the internal or external medium. Intracellular H-7, staurosporine, IP3, cAMP, cGMP, or calmodulin inhibitors failed to prevent the quisqualate-induced Ca2+ current inhibition. These observations are consistent with an interaction between a G protein-coupled glutamate receptor and Ca2+ channels.",

author = "Lester, \{Robin A.J.\} and Jahr, \{Craig E.\}",

note = "Funding Information: We thank Mr. Jeff Volk for the preparation and maintenance of the neurons and Drs. J. T. Williams and C. L. Westbrook for careful reading and criticism of the manuscript. In separate experiments performed by Dr. M. J. Christie IP, induced an oscillatory Cl-conductance in Xenopus oocytes, confirming the activity of the compound. This work was supported by National Institutes of Health grant NS21419 and the McKnight Endowment Fund for Neuroscience.",

year = "1990",

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doi = "10.1016/0896-6273(90)90200-Y",

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AU - Jahr, Craig E.

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PY - 1990/5

Y1 - 1990/5

N2 - The modulation of Ca2+ currents by the excitatory neurotransmitter glutamate and its analogs was investigated in hippocampal neurons in culture. In the presence of glutamate receptor-gated ion channel antagonists, all of the analogs tested caused either a small reversible depression or had no effect on the Ca2+ current. However, in neurons dialyzed with GTPyS, quisqualate and glutamate but not NMDA, kainate, AMPA, or l-APB caused marked and irreversible depressions of the Ca2+ current. This inhibition was only observed if Ca2+ was present in either the internal or external medium. Intracellular H-7, staurosporine, IP3, cAMP, cGMP, or calmodulin inhibitors failed to prevent the quisqualate-induced Ca2+ current inhibition. These observations are consistent with an interaction between a G protein-coupled glutamate receptor and Ca2+ channels.

AB - The modulation of Ca2+ currents by the excitatory neurotransmitter glutamate and its analogs was investigated in hippocampal neurons in culture. In the presence of glutamate receptor-gated ion channel antagonists, all of the analogs tested caused either a small reversible depression or had no effect on the Ca2+ current. However, in neurons dialyzed with GTPyS, quisqualate and glutamate but not NMDA, kainate, AMPA, or l-APB caused marked and irreversible depressions of the Ca2+ current. This inhibition was only observed if Ca2+ was present in either the internal or external medium. Intracellular H-7, staurosporine, IP3, cAMP, cGMP, or calmodulin inhibitors failed to prevent the quisqualate-induced Ca2+ current inhibition. These observations are consistent with an interaction between a G protein-coupled glutamate receptor and Ca2+ channels.

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Quisqualate receptor-mediated depression of calcium currents in hippocampal neurons

Abstract

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ASJC Scopus subject areas

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